cardio i - jan 2015
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CARDIOLOGY I MASON COUNTY EMS ALS/ILS OTEP Topics Review of Cardiovascular Anatomy Cardiac Physiology Electrocardiographic Monitoring Dysrhythmias Cardiovascular Anatomy Blood Flow From the Body • Right Atrium To the Lungs • Right Ventricle From the Lungs • Left Atrium To the Body • Left Ventricle Cardiovascular Anatomy Coronary Circulation Collateral Circulation Cardiac Physiology The Cardiac Cycle Diastole Systole Ejection Fraction Stroke Volume • Preload • Cardiac Contractility • Afterload Cardiac Output Cardiac Physiology Electrophysiology Cardiac Muscle Atrial Ventricular Excitatory and Conductive Fibers • Intercalated discs • Syncytium Atrioventricular Bundle Depolarization Cardiac Physiology Cardiac Depolarization Resting Potential Action Potential Repolarization Cardiac Physiology Cardiac Conductive System Properties • • • • Excitability Conductivity Automaticity Contractility Cardiac Physiology Cardiac Conductive System Components • Sinoatrial Node • Internodal Atrial Pathways • Atrioventricular Node • Atrioventricular Junction • Bundle of His • Left and Right Bundle Branches • Purkinje Fibers Electrocardiographic Monitoring The Electrocardiogram Positive and Negative Impulses The Isoelectric Line Artifact Muscle tremors Shivering Patient movement Loose electrodes 60 Hertz interference Machine malfunction The Electrocardiogram ECG Leads Bipolar (Limb) Einthoven’s Triangle Leads I, II, III Augmented (Unipolar) aVR, aVL, aVF Precordial V1 – V6 The Electrocardiogram The Electrocardiogram Routine Monitoring Information from a single lead shows: Rate & regularity. Time to conduct an impulse. A single lead cannot: Identify/locate an infarct. Identify axis deviation or chamber enlargement. Identify right-to-left differences in conduction. The quality or presence of pumping action. The Electrocardiogram ECG Paper Speed Amplitude and Deflection Calibration The Electrocardiogram Relationship of the ECG to Electrical Events in the Heart ECG Components P Wave QRS Complex T Wave U Wave The Electrocardiogram The Electrocardiogram The Electrocardiogram The Electrocardiogram The Electrocardiogram The Electrocardiogram The Electrocardiogram The Electrocardiogram Time Intervals P–R Interval (PRI) or P–Q Interval (PQI) • 0.12–0.20 Seconds QRS Interval • 0.08–0.12 Seconds S–T Segment Q–T Interval • 0.33–0.42 Seconds The Electrocardiogram Refractory Periods Absolute Relative The Electrocardiogram S–T Segment Changes Associated with Myocardial Infarctions Ischemia Injury Necrosis The Electrocardiogram Lead Systems and Heart Surfaces The Electrocardiogram Interpretation of Rhythm Strips Basic Criteria Always be consistent and analytical. Memorize the rules for each dysrhythmia. Analyze a given rhythm strip according to a specific format. Compare your analysis to the rules for each dysrhythmia. Identify the dysrhythmia by its similarity to established rules. The Electrocardiogram Five-Step Procedure Analyze the rate. Analyze the rhythm. Analyze the P-waves. Analyze the P–R interval. Analyze the QRS complex. The Electrocardiogram Analyzing Rate Six-Second Method Heart Rate Calculator Rulers R–R Interval Triplicate Method Analyzing Rhythm Regular Occasionally Irregular Regularly Irregular Irregularly Irregular The Electrocardiogram Analyzing P Waves Are P waves present? Are the P waves regular? Is there one P wave for each QRS complex? Are the P waves upright or inverted? Do all the P waves look alike? Analyzing the P–R Interval Analyzing the QRS Complex Do all the QRS complexes look alike? What is the QRS duration? Dysrhythmias Normal Sinus Rhythm Rate 60–100 Rhythm Regular P waves Normal, upright, only before each QRS complex PR Interval 0.12–0.20 seconds QRS Complex Normal, duration of <0.12 seconds Causes of Dysrhythmias Myocardial Ischemia, Necrosis, or Infarction Autonomic Nervous System Imbalance Distention of the Chambers of the Heart Blood Gas Abnormalities Electrolyte Imbalances Trauma to the Myocardium Drug Effects and Drug Toxicity Electrocution Hypothermia CNS Damage Idiopathic Events Normal Occurrences Dysrhythmias Dysrhythmia Arrhythmia Mechanism of Impulse Formation Ectopic Foci Ectopic Beats Reentry Dysrhythmias Classification of Dysrhythmias Nature of Origin Magnitude Severity Site of Origin Dysrhythmias Classification by Site of Origin Dysrhythmias Originating in the SA Node Dysrhythmias Originating in the Atria Dysrhythmias Originating Within the AV Junction (AV Blocks) Dysrhythmias Sustained in or Originating in the AV Junction Dysrhythmias Originating in the Ventricles Dysrhythmias Resulting from Disorders of Conduction Dysrhythmias Originating in the SA Node Sinus Bradycardia Sinus Tachycardia Sinus Dysrhythmia Sinus Arrest Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus Bradycardia Rate Rhythm Pacemaker Site P Waves Less than 60 Regular SA node Upright & normal PRI Normal QRS Normal Dysrhythmias Originating in the SA Node Sinus Bradycardia Etiology Increased parasympathetic (vagal) tone, intrinsic disease of the SA node, drug effects. May be a normal finding in healthy, well-conditioned persons. Clinical Significance May result in decreased cardiac output, hypotension, angina, or CNS symptoms. In healthy, well-conditioned person, may have no significance. Treatment Generally unnecessary unless hypotension or ventricular irritability is present. Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus Tachycardia Rate Rhythm Pacemaker Site P Waves Greater than 100 Regular SA node Upright & normal PRI Normal QRS Normal Dysrhythmias Originating in the SA Node Sinus Tachycardia Etiology Results from an increased rate of SA node discharge. Potential causes include exercise, fever, anxiety, hypovolemia, anemia, pump failure, increased sympathetic tone, hypoxia, or hypothyroidism. Clinical Significance Decreased cardiac output for rates >140. Very rapid rates can precipitate ischemia or infarct. Treatment Treatment is directed at the underlying cause. Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus Dysrhythmia Rate Rhythm Pacemaker Site P Waves 60–100 Irregular SA node Upright & normal PRI Normal QRS Normal Dysrhythmias Originating in the SA Node Sinus Dysrhythmia Etiology Often a normal finding, sometimes related to the respiratory cycle. May be caused by enhanced vagal tone. Clinical Significance Normal variant. Treatment Typically, none required. Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus Arrest Rate Rhythm Pacemaker Site P Waves Normal to slow Irregular SA node Upright & normal PRI Normal QRS Normal Dysrhythmias Originating in the SA Node Sinus Arrest Etiology Occurs when the sinus node fails to discharge. May result from ischemia of the SA node, digitalis toxicity, excessive vagal tone, or degenerative fibrotic disease. Clinical Significance Frequent or prolonged episodes may decrease cardiac output and cause syncope. Prolonged episodes may result in escape rhythms. Treatment None if patient is asymptomatic. Treat symptomatic bradycardia. Dysrhythmias Originating in the Atria Atrial Tachycardia Multifocal Atrial Tachycardia Premature Atrial Contractions Paroxysmal Supraventricular Tachycardia Atrial Flutter Atrial Fibrillation Dysrhythmias Originating in the Atria Rules of Interpretation Atrial Tachycardia Rate Rhythm Pacemaker Site P Waves PRI QRS Usually normal Slightly irregular Varies among the SA node, atrial tissue, and AV Junction Variable or absent Varies depending on source of impulse Normal Dysrhythmias Originating in the Atria Atrial Tachycardia Etiology Variant of sinus dysrhythmia, which is a natural phenomenon in the very young or old. May also be caused by ischemic heart disease or atrial dilation. Clinical Significance None, but may be precursor to other atrial dysrhythmias. Treatment Typically, none required. Dysrhythmias Originating in the Atria Rules of Interpretation Multifocal Atrial Tachycardia Rate Rhythm More than 100 Irregular Pacemaker Site Ectopic sites in atria P Waves Organized, nonsinus P waves; at least 3 forms PRI Varies depending on source of impulse QRS Variable Dysrhythmias Originating in the Atria Multifocal Atrial Tachycardia Etiology Often seen in acutely ill patients. May result from pulmonary disease, metabolic disorders, ischemic heart disease, or recent surgery. Clinical Significance Presence of multifocal atrial tachycardia often indicates a serious underlying illness. Treatment Treat the underlying illness. Dysrhythmias Originating in the Atria Rules of Interpretation Premature Atrial Contractions Rate Depends on underlying rhythm Rhythm Usually regular except for the PAC Pacemaker Site P Waves PRI QRS Ectopic sites in atria Occurs earlier than expected Varies dependent on foci of impulse Usually normal Dysrhythmias Originating in the Atria Premature Atrial Contractions Etiology Single electrical impulse originating outside the SA node. May result from use of caffeine, tobacco, or alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic. Clinical Significance None. Presence of PACs may be a precursor to other atrial dysrhythmias. Treatment None if asymptomatic. Treat symptomatic patients by administering high-flow oxygen and establishing IV access. Dysrhythmias Originating in the Atria Rules of Interpretation Paroxysmal Supraventricular Tachycardia Rate 150–250 Rhythm Regular Pacemaker Site P Waves Atrial (outside SA Node) Often buried in preceding T wave PRI Usually normal QRS Usually normal Dysrhythmias Originating in the Atria Paroxysmal Supraventricular Tachycardia Etiology Rapid atrial depolarization overrides the SA node. May be precipitated by stress, overexertion, smoking, caffeine. Clinical Significance May be tolerated well by healthy patients for short periods. Marked reduction in cardiac output can precipitate angina, hypotension, or congestive heart failure. Dysrhythmias Originating in the Atria Paroxysmal Supraventricular Tachycardia Treatment Vagal Maneuvers Pharmacological Therapy • Adenosine • Verapamil Electrical Therapy • Consider if patient symptomatic with HR > 150. • Synchronized cardioversion starting at 100J. Dysrhythmias Originating in the Atria Rules of Interpretation Atrial Flutter Rate Rhythm Pacemaker Site P Waves Atrial rate 250–350 Ventricular rate varies Usually regular Atrial (outside SA node) F waves are present PRI Usually normal QRS Usually normal Dysrhythmias Originating in the Atria Atrial Flutter Etiology Results when the AV node cannot conduct all the impulses. Impulses may be conducted in fixed or variable ratios. Usually associated with organic disease such as congestive heart failure (rarely seen with MI). Clinical Significance Generally well tolerated. Rapid ventricular rates may compromise cardiac output and result in symptoms. May occur in conjunction with atrial fibrillation. Dysrhythmias Originating in the Atria Atrial Flutter Treatment Electrical Therapy • Consider if ventricular rate > 150 and symptomatic. • Synchronized cardioversion starting at 100J. Pharmacological Therapy • Diltiazem. • Verapamil, digoxin, beta-blockers, procainamide, and quinidine. Dysrhythmias Originating in the Atria Rules of Interpretation Atrial Fibrillation Rate Atrial rate 350–50 Ventricular rate varies Rhythm Irregularly irregular Pacemaker Site P Waves PRI QRS Atrial (outside SA Node) None discernible None Normal Dysrhythmias Originating in the Atria Atrial Fibrillation Etiology Results from multiple ectopic foci; AV conduction is random and highly variable. Often associated with underlying heart disease. Clinical Significance Atria fail to contract effectively, reducing cardiac output. Well tolerated with normal ventricular rates. High or low ventricular rates can result in cardiac compromise. Dysrhythmias Originating in the Atria Atrial Fibrillation Treatment Electrical Therapy • Consider if ventricular rate > 150 and symptomatic. • Synchronized cardioversion starting at 100J. Pharmacological Therapy • Diltiazem. • Verapamil, digoxin, beta blockers, procainamide, and quinidine. • Anticoagulant (heparin or warfarin). Dysrhythmias Originating Within the AV Junction (AV Blocks) AV Blocks Locations At the AV Node At the Bundle of His Below the Bundle of His Classifications First-Degree AV Block Type I Second-Degree AV Block Type II Second-Degree AV Block Third-Degree AV Block Dysrhythmias Originating Within the AV Junction (AV Blocks) Rules of Interpretation First-Degree AV Block Rate Rhythm Pacemaker Site P Waves PRI QRS Depends on underlying rhythm Usually regular SA node or atrial Normal > 0.20 Seconds Usually < 0.12 seconds Dysrhythmias Originating Within the AV Junction (AV Blocks) First-Degree AV Block Etiology Delay in the conjunction of an impulse through the AV node. May occur in healthy hearts, but often indicative of ischemia at the AV junction. Clinical Significance Usually not significant, but new onset may precede a more advanced block. Treatment Generally, none required other than observation. Avoid drugs that may further slow AV conduction. Dysrhythmias Originating Within the AV Junction (AV Blocks) Rules of Interpretation Type I Second-Degree AV Block Rate Rhythm Pacemaker Site Atrial, normal; ventricular, normal to slow Atrial, regular; ventricular, irregular SA node or arial P Waves Normal, some P waves not followed by QRS PRI Increases until QRS is dropped, then repeats QRS Usually < 0.12 seconds Dysrhythmias Originating Within the AV Junction (AV Blocks) Type I Second-Degree AV Block Etiology Also called Mobitz I, or Wenckebach. Delay increases until an impulse is blocked. Indicative of ischemia at the AV junction. Clinical Significance Frequently dropped beats can result in cardiac compromise. Treatment Generally, none required other than observation. Avoid drugs that may further slow AV conduction. Treat symptomatic bradycardia. Dysrhythmias Originating Within the AV Junction (AV Blocks) Rules of Interpretation Type II Second-Degree AV Block Rate Rhythm Pacemaker Site P Waves PRI QRS Atrial, normal; ventricular, slow May be regular or irregular SA node or atrial Normal, some P waves not followed by QRS Constant for conducted beats, may be > 0.21 seconds Normal or > 0.12 seconds Dysrhythmias Originating Within the AV Junction (AV Blocks) Type II Second-Degree AV Block Etiology Also called Mobitz II or infranodal. Intermittent block of impulses. Usually associated with MI or septal necrosis. Clinical Significance May compromise cardiac output and is indicative of MI. Often develops into full AV blocks. Treatment Avoid drugs that may further slow AV conduction. Treat symptomatic bradycardia. Consider transcutaneous pacing. Dysrhythmias Originating Within the AV Junction (AV Blocks) Rules of Interpretation Third-Degree AV Block Rate Rhythm Pacemaker Site P Waves PRI QRS Atrial, normal; ventricular, 40–60 Both atrial and ventricular are regular SA node and AV junction or ventricle Normal,with no correlation to QRS No relationship to QRS 0.12 seconds or greater Dysrhythmias Originating Within the AV Junction (AV Blocks) Third-Degree AV Block Etiology Absence of conduction between the atria and the ventricles. Results from AMI, digitalis toxicity, or degeneration of the conductive system. Clinical Significance Severely compromised cardiac output. Treatment Transcutaneous pacing for acutely symptomatic patients. Treat symptomatic bradycardia. Avoid drugs that may further slow AV conduction. Dysrhythmias Sustained or Originating in the AV Junction Dysrhythmias Premature Junctional Contractions Junctional Escape Complexes and Rhythm Accelerated Junctional Rhythm Paroxysmal Junctional Tachycardia Characterisitics Inverted P Waves in Lead II PRI of < 0.12 Seconds Normal QRS Complex Duration Dysrhythmias Sustained or Originating in the AV Junction Rules of Interpretation Premature Junctional Contractions Rate Rhythm Pacemaker Site P Waves PRI QRS Depends on underlying rhythm Depends on underlying rhythm Ectopic focus in the AV junction Inverted, may occur after QRS Normal if P occurs before QRS Usually normal Dysrhythmias Sustained or Originating in the AV Junction Premature Junctional Contractions Etiology Single electrical impulse originating in the AV node. May occur with use of caffeine, tobacco, alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic. Clinical Significance Limited, frequent PJCs may precursor other junctional dysrhythmias. Treatment None usually required. Dysrhythmias Sustained or Originating in the AV Junction Rules of Interpretation Junctional Escape Complexes and Rhythms Rate Rhythm Pacemaker Site P Waves PRI QRS 40–60 Irregular in single occurrence, regular in escape rhythm AV junction Inverted, may occur after QRS Normal if P occurs before QRS Usually normal Dysrhythmias Sustained or Originating in the AV Junction Junctional Escape Complexes and Rhythms Etiology Results when the AV node becomes the pacemaker. Results from increased vagal tone, pathologically slow SA discharges, or heart block. Clinical Significance Slow rate may decrease cardiac output, precipitating angina and other problems. Treatment None if the patient remains asymptomatic. Treat symptomatic episodes with atropine or pacing as indicated. Dysrhythmias Sustained or Originating in the AV Junction Rules of Interpretation Accelerated Junctional Rhythm Rate Rhythm Pacemaker Site P Waves PRI QRS 60–100 Regular AV junction Inverted, may occur after QRS Normal if P occurs before QRS Normal Dysrhythmias Sustained or Originating in the AV Junction Accelerated Junctional Rhythm Etiology Results from increased automaticity in the AV junction. Often occurs due to ischemia of the AV junction. Clinical Significance Usually well tolerated, but monitor for other dysrhythmias. Treatment None generally required in the prehospital setting. Dysrhythmias Sustained or Originating in the AV Junction Rules of Interpretation Paroxysmal Junctional Tachycardia Rate 100–180 Rhythm Regular Pacemaker Site P Waves PRI QRS AV junction Inverted, may occur after QRS Normal if P occurs before QRS Normal Dysrhythmias Sustained or Originating in the AV Junction Paroxysmal Junctional Tachycardia Etiology Rapid AV junction depolarization overrides the SA node. Occurs with or without heart disease. May be precipitated by stress, overexertion, smoking, or caffeine ingestion. Clinical Significance May be well tolerated for brief periods. Decreased cardiac output will result from prolonged episodes, which may precipitate angina, hypotension, or congestive heart failure. Dysrhythmias Sustained or Originating in the AV Junction Paroxysmal Junctional Tachycardia Treatment Vagal Maneuvers Pharmacological Therapy • Adenosine • Verapamil Electrical Therapy • Use if rate is > 150 and patient is hemodynamically unstable. • Synchronized cardioversion starting at 100J. Dysrhythmias Originating in the Ventricles Dysrhythmias Ventricular Escape Complexes and Rhythms Accelerated Idioventricular Rhythm Premature Ventricular Contractions Ventricular Tachycardia Related Dysrhythmia Ventricular Fibrillation Asystole Artificial Pacemaker Rhythm Dysrhythmias Originating in the Ventricles Rules of Interpretation Ventricular Escape Complexes and Rhythms Rate Rhythm Pacemaker Site 15–40 Escape complex, irregular; escape rhythm, Regular Ventricle P Waves None PRI None QRS >0.12 seconds, bizarre Dysrhythmias Originating in the Ventricles Ventricular Escape Complexes and Rhythms Etiology Safety mechanism to prevent cardiac standstill. Results from failure of other foci or high-degree AV block. Clinical Significance Decreased cardiac output, possibly to life-threatening levels. Treatment For perfusing rhythms, administer atropine and/or TCP. For nonperfusing rhythms, follow pulseless electrical activity (PEA) protocols. Dysrhythmias Originating in the Ventricles Accelerated Idioventricular Rhythm Etiology A subtype of ventricular escape rhythm that frequently occurs with MI. Ventricular escape rhythm with a rate of 60–110. Clinical Significance May cause decreased cardiac output if the rate slows. Treatment Does not usually require treatment unless the patient becomes hemodynamically unstable. Primary goal is to treat the underlying MI. Dysrhythmias Originating in the Ventricles Rules of Interpretation Premature Ventricular Contractions Rate Underlying rhythm Rhythm Interrupts regular underlying rhythm Pacemaker Site Ventricle P Waves None PRI None QRS >0.12 seconds, bizarre Dysrhythmias Originating in the Ventricles Premature Ventricular Contractions Etiology Single ectopic impulse resulting from an irritable focus in either ventricle. Causes may include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid–base disturbances, electrolyte imbalances, or as a normal variation of the ECG. May occur in patterns • Bigeminy, trigeminy, or quadrigeminy. • Couplets and triplets. Dysrhythmias Originating in the Ventricles Premature Ventricular Contractions Clinical Significance Malignant PVCs • More than 6/minute, R on T phenomenon, couplets or runs of ventricular tachycardia, multifocal PVCs, or PVCs associated with chest pain. Ventricles do not adequately fill, causing decreased cardiac output. Dysrhythmias Originating in the Ventricles Premature Ventricular Contractions Treatment Non-malignant PVCs do not usually require treatment in patients without a cardiac history. Cardiac patient with nonmalignant PVCs . • Administer oxygen and establish IV access Malignant PVCs: • Lidocaine 1.0 –1.5 mg/kg IV bolus. • If PVCs are not suppressed, repeat doses of 0.5-0.75 mg/kg to max dose of 3.0 mg/kg. • If PVCs are suppressed, administer lidocaine drip 2–4 mg/min. • Reduce the dose in patients with decreased output or decreased hepatic function and patients > 70 years old. Dysrhythmias Originating in the Ventricles Rules of Interpretation Ventricular Tachycardia Rate Rhythm Pacemaker Site P Waves PRI QRS 100–250 Usually regular Ventricle If present, not associated with QRS None >0.12 seconds, bizarre Dysrhythmias Originating in the Ventricles Ventricular Tachycardia Etiology 3 or more ventricular complexes in succession at a rate of >100. Causes include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid–base disturbances, or electrolyte imbalances. VT may appear monomorphic or polymorphic Clinical Significance Decreased cardiac output, possibly to life-threatening levels. May deteriorate into ventricular fibrillation. Dysrhythmias Originating in the Ventricles Ventricular Tachycardia Treatment Perfusing patient • Administer oxygen and establish IV access. • Consider immediate synchronized cardioversion starting at 100J for hemodynamically unstable patients. • Initially administer lidocaine 1.0–1.5 mg/kg IV. • Administer repeat doses of lidocaine 0.5–0.75 mg/kg to the max dose of 3.0 mg/kg, or until VT is suppressed. • Amiodarone 150–300 mg IV. Nonperfusing patient • Follow ventricular fibrillation protocol. Dysrhythmias Originating in the Ventricles Torsade de Pointes Polymorphic VT. Caused by the use of certain antidysrhythmic drugs. Exacerbated by coadministration of antihistamines, azole antifungal agents and macrolide antibiotics, erythromycin, azithromycin, and clarithramycin. Dysrhythmias Originating in the Ventricles Torsade de Pointes Typically occurs in nonsustained bursts. Prolonged Q–T interval during “breaks.” QRS rates from 166–300. RR interval highly variable. Treatment Do not treat as standard VT. Administer magnesium sulfate 1–2 g diluted in 100 ml D5W over 1–2 minutes. Amiodarone 150–300 mg is also effective. Dysrhythmias Originating in the Ventricles Rules of Interpretation Ventricular Fibrillation Rate No organized rhythm Rhythm No organized rhythm Pacemaker Site Numerous ventricular foci P Waves Usually absent PRI None QRS None Dysrhythmias Originating in the Ventricles Ventricular Fibrillation Etiology Wide variety of causes, often resulting from advanced coronary artery disease. Clinical Significance Lethal dysrhythmia with no cardiac output and no organized electrical pattern. Dysrhythmias Originating in the Ventricles Ventricular Fibrillation Treatment Initiate CPR. Defibrillate with 200J, repeated with 200–300J and 360J if the rhythm does not convert. Control the airway and establish IV access. Administer epinephrine 1:10,000 every 3–5 minutes. Consider second-line drugs such as lidocaine, bretylium, amiodarone, procainamide, or magnesium sulfate. Consider 40 IU Vasopressin IV (one time only). Dysrhythmias Originating in the Ventricles Rules of Interpretation Asystole Rate No Electrical Activity Rhythm No Electrical Activity Pacemaker Site No Electrical Activity P Waves Absent PRI Absent QRS Absent Dysrhythmias Originating in the Ventricles Asystole Etiology Primary event in cardiac arrest, resulting from massive myocardial infarction, ischemia, and necrosis. Final outcome of ventricular fibrillation. Clinical Significance Asystole results in cardiac arrest. Poor prognosis for resuscitation. Dysrhythmias Originating in the Ventricles Asystole Treatment Administer CPR and manage the airway. Treat for ventricular fibrillation if there is any doubt about the underlying rhythm. Administer medications • Epinephrine, atropine, and possibly sodium bicarbonate. Dysrhythmias Originating in the Ventricles Rules of Interpretation Artificial Pacemaker Rhythm Rate Rhythm Varies with pacemaker May be regular or irregular Pacemaker Site Depends upon electrode placement P Waves None produced by ventricular pacemakers; pacemaker spike PRI QRS If present, varies >0.12 seconds, bizarre Dysrhythmias Originating in the Ventricles Artificial Pacemaker Rhythm Etiology Single vs. dual chamber pacemakers. Fixed-rate vs. demand pacemakers. Clinical Significance Used in patients with a chronic high-–grade heart block, sick sinus syndrome, or severe symptomatic bradycardia. Dysrhythmias Originating in the Ventricles Artificial Pacemaker Rhythm Problems with Pacemakers Battery failure “Runaway” pacers Displaced leads Management Considerations Identify patients with pacemakers. Treat the patient. Use of a Magnet Pulseless Electrical Activity Characteristics Electrical impulses are present, but with no accompanying mechanical contractions of the heart. Treat the patient, not the monitor. Causes Hypovolemia, cardiac tamponade, tension pneumothorax, hypoxemia, acidosis, massive pulmonary embolism, ventricular wall rupture. Pulseless Electrical Activity Treatment Prompt recognition and early treatment. Epinephrine 1 mg every 3–5 minutes. Treat underlying cause of PEA. Dysrhythmias Resulting from Disorders of Conduction Categories of Conductive Disorders Atrioventricular Blocks Disturbances of Ventricular Conduction Preexcitation Syndromes Dysrhythmias Resulting from Disorders of Conduction Disturbances of Ventricular Conduction Aberrant Conduction Bundle Branch Block Causes Ischemia or necrosis of a bundle branch PAC or PJC that reaches one of the bundle branches in a refractory period Differentiation of SVT and Wide-Complex Tachycardias Dysrhythmias Resulting from Disorders of Conduction Pre-excitation Syndromes Excitation by an impulse that bypasses the AV node Wolff-Parkinson-White Syndrome (WPW) • Short PRI and long QRS duration • Delta waves Treat underlying rhythm. ECG Changes Due to Electrolyte Abnormalities and Hypothermia Hyperkalemia Tall Ts Suspect in patients with a history of renal failure. Hypokalemia Prominent U waves Hypothermia Osborn wave (“J” wave) T wave inversion, sinus bradycardia, atrial fibrillation or flutter, AV blocks, PVCs, VF, asystole Summary Review of Cardiovascular Anatomy Cardiac Physiology Electrocardiographic Monitoring Dysrhythmias
